Allergic diseases are a major health problem as a very great number of individuals are affected thereby. Usually the therapy is restricted to the use of antihistamines or to more or less effective immunization procedures. The classical antiallergic drugs have certain disadvantages, especially since they cause various side effects in the treated patient. The immunization procedure is limited to one or two allergens whereas most of the patients are sensitive to a large number of allergens. In addition, hyposensitization treatment is neither curative nor protective. As it is known that IgE plays a major role in allergic diseases, the mechanisms regulating the production of IgE have been extensively investigated during the last ten years. These studies have demonstrated the existence in animal models of several factors controlling the synthesis of IgE. Such factors are produced by B and T lymphocytes and have been named: suppressing factor of allergy (SFA), suppressive effector molecules (SEM), IgE-induced regulants from B or T cells (EIR.sub.B and EIR.sub.T) IgE-binding factors (IgE-BFs), glycosylation enhancing factors (GEF), and glycosylation inhibiting factors (GIF).
Some of the factors are definitely different from each other on account of their molecular weights and/or biological activities (for review see references 1 and 2).
The role of IgE-binding factors (IgE-bfs) in the non-antigen specific regulation of IgE antibody production has been extensively investigated in animals (as reviewed in reference 1) where it was shown that IgE-bfs are the effector molecules of the IgE-specific isotype regulation. Two kinds of IgE-bfs differing mainly by their carbohydrate moieties were identified, i.e. IgE suppressor and IgE potentiating factors (IgE-SFs; IgE-PFs); the ratio between IgE-SFs and IgE-PFs determines the actual production of IgE antibodies. The same cells are capable of secreting either IgE-SFs or IgE-PFs depending on the influence of either glycosylation inhibiting or enhancing factors (GIF, GEF) which are secreted by distinct regulatory T lymphocyte subpopulations.
Human IgE-bfs have also been described recently in the culture supernatants of either T- or B-cell lines expressing receptors for IgE (3, 4) as well as in the serum of selected patients with severe atopic dermatitis (5). Further biochemical characterization of the IgE-bfs of different origins is definitely required in order to determine whether or not they correspond to identical molecules. It is already known that breast-feeding may alter the immune reactivity of the newborn. This was described in experimental animals (6) and in humans where it was shown, for example, that babies fed with milk from tuberculin sensitive mothers acquired cell-mediated immunity to tuberculin (7,8). Recent prospective studies further indicated that exclusive breast-feeding protects the high risk infants against allergic disease.
Multiple mechanisms were invoked to explain the latter observations: (i) a reduced exposure to foreign food antigens, (ii) the protection by milk IgA blocking antibodies specific to various alimentary antigens and to other environmental antigens (9), (iii) the protection against common viral diseases known to trigger the onset of allergic diseases (10) and finally (iv) the presence in human milk of immunoregulatory factors capable of modulating the immature immune system of the neonate (11). It is also known that newborns with a high risk for allergic diseases can be identified on the basis of family history and of high IgE levels in the cord blood serum (12).
The well documented observation on the immunoreactivity of breast-fed newborns might be explained by the presence in human colostrum of specific antibodies or idiotypes (13, 14), immunoregulatory factors, or regulatory lymphocytes (15, 16). Hence, it is suggested that breast-feeding may protect newborns by providing them with either IgE-suppressor factors, or with other molecules (such as GIF) or cells capable of interfering with the infants lymphocytes involved in the regulation of IgE antibody production.
So far IgE-bfs with IgE-SF activity have not been identified in human colostrum, and the isolation thereof is nowhere described. Surprisingly, such IgE-bfs have now been isolated.